Myocardial insulin resistance contributes to the development of diabetic cardiomyopathy by altering myocardial energy metabolism, intracellular calcium handling, and cell survival.
Heart disease is the leading cause of death in patients with insulin resistance and type 2 diabetes (DM2). Even in the absence of coronary artery disease and hypertension, functional and structural abnormalities exist in patients with well-controlled and uncomplicated DM2. These derangements are collectively designated by the term diabetic cardiomyopathy (DCM). Changes in myocardial energy metabolism, due to altered substrate supply and utilization, largely underlie the development of DCM. Insulin is an important regulator of myocardial substrate metabolism, but also exerts regulatory effects on intracellular Ca2+ handling and cell survival. The current paper reviews the multiple functional and molecular effects of insulin on the heart, all of which ultimately seem to be cardioprotective both under normal conditions and under ischemia. In particular, the dismal consequences of myocardial insulin resistance contributing to the development of DCM will be discussed.
Ouwens et al. (Mon,) conducted a review in Diabetic cardiomyopathy and insulin resistance. Insulin was evaluated. Myocardial insulin resistance contributes to the development of diabetic cardiomyopathy by altering myocardial energy metabolism, intracellular calcium handling, and cell survival.